This study will determine whether enigmatic clinical outcomes in patients with galactosemia, who have identical molecular and biochemical mutations in red blood cell galactose-1-phosphate uridyltransferase (GALT), are caused by alternative pathways and organ-specific impairment for galactose metabolism. The hypothesis will be tested by quantitative and qualitative comparisons of in vivo galactose metabolic pathways in patients with galactosemia who are homozygous for the Q188R mutation, or have other defined mutations.